Cariogenic potential of pooled plaque fluid from exposed root surfaces in humans

Margolis, Henry C.; Zhang, Y.P.; Gewirtz, Andrew T.; Houte, J. van; Moreno, E.C.

doi:10.1016/0003-9969(93)90197-t

Cited by 17 publications

(12 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The observed concentrations of formic and acetic acid were unexpectedly high at baseline levels (table 4). Other investigators found similar concentrations of organic acids in starved plaque fluid [17,18]. These acids could have originated either from the metabolism of carbohydrates in food remnants or from soluble polysaccharides stored or retained in plaque, such as levan and starch.…”

Section: Discussionmentioning

confidence: 86%

Clearance and Metabolism of Starch Foods in the Oral Cavity

Linke

Birkenfeld²

1999

Ann Nutr Metab

View full text Add to dashboard Cite

The presence of carbohydrates and organic acids was monitored in the oral cavity over a 3-hour period following the ingestion of six foods containing cooked starch (popcorn, potato chips, corn flakes, bread stick, hard pretzel and wheat cracker) and compared to a food containing sugar (chocolate-covered candy bar). Oral fluid samples were collected at 30-min intervals from five different tooth sites from 7 volunteers using absorbent paper points. Samples were analyzed for carbohydrates and organic acids using high-performance liquid chromatography. Analytical data for each food were pooled and compared to the results of the sugar food. The amount of lactic acid produced 30 min after ingestion was highest with the potato chips and lowest with the corn flakes. Potato starch contributed more readily to oral lactic acid production than wheat or corn starch. A direct linear relationship existed between lactic acid production and the presence of oral glucose produced from starch, which occurred via the metabolites maltotriose and maltose. Oral clearance of foods containing cooked starch proceeded significantly slower than that of the sugar food, thus contributing to a prolonged period of lactic acid production.

show abstract

Section: Discussionmentioning

confidence: 86%

Clearance and Metabolism of Starch Foods in the Oral Cavity

Linke

Birkenfeld²

1999

Ann Nutr Metab

View full text Add to dashboard Cite

show abstract

“…Parallel work by of Geddes (1975) and Gilmour (1976) demonstrated the generation of several SCCA by dental plaque in situ. Investigators then found that SCCA concentrations increased after administration of sugar rinses (Vratsanos and Mandel, 1982;Margolis et al, 1993) and foods (Kashket et al, 1991(Kashket et al, , 1996. In particular, Kashket et al (I 996) noted that following food ingestion, food particles are retained on the dentition between the teeth and at the gingival margins for relatively long periods of time, and salivary micro-organisms entrapped within the food particles generate mM levels of formic, acetic, lactic, and propionic acids.…”

Section: Short-chain Carboxylic Acid Generation By Periodontal Microbmentioning

confidence: 99%

“…Mayhew et al, 1975;Gorbach et al, 1976;Ladas et al, 1979). Over the next 20 years, these microbiological methods were further refined, the experiments repeated, and the results verified by a number of other investigators examining oral microbes (e.g., Geddes, 1975;Gilmour., 1976;Touw et al, 1982;Vratsanos and Mandel, 1982;van Steenbergen et al, 1986;Moreno and Margolis, 1988;Lucarelli et al, 1990;Margolis et al, 1993;Kurita-Ochiai et al, 1995). The concentration ranges and the ratios of SCCA varied somewhat with each investigation.…”

Section: Short-chain Carboxylic Acid Generation By Periodontal Microbmentioning

confidence: 99%

Short-Chain Carboxylic-Acid-Stimulated, PMN-Mediated Gingival Inflammation

Niederman

Zhang²,

Kashket³

1997

Critical Reviews in Oral Biology & Medicine

121

105

View full text Add to dashboard Cite

This communication reviews the effects of short-chain carboxylic acids on human cells of importance to the periodontium. The central hypothesis is that these acids can alter both cell function and gene expression, and thus contribute to the initiation and prolongation of gingival inflammation.Short-chain carboxylic acids [CH3-(CH2)x-COOH, x < 31 are metabolic intermediates with a broad range of apparently paradoxical biological effects. For example, lactic acid (CH3-CHOH-COOH), a 3-carbon alpha-hydroxy-substituted acid, is widely recognized for its cariogenicity. Lactic acid, however, also occurs in tropical fruits, and is the active ingredient in a variety of anti-wrinkle creams developed by dermatologists. In marked contrast, the unsubstituted 3-carbon propionic acid (CH3-CH2-COOH) is used as a food preservative and is the active principle for one class of non-steroidal anti-inflammatory agents. Interestingly, the addition of one carbon to propionic acid dramatically changes the biological effects. The unsubstituted 4-carbon butyric acid (CH3-CH2-CH 2-COOH) is used by hematologists as a de-differentiating agent for the treatment of sickle cell anemia, but by oncologists as a differentiating agent for cancer chemotherapy. Finally, acting either individually or in concert, these acids can increase vascular dilation. Clearly, these acids, while metabolically derived, have a number of very divergent activities which are cell-type-specific (Fig. 1).It may be telling that periodontal bacteria produce these acids in millimolar concentrations, and that these bacteria can be characterized by their acid production profiles. It is no less interesting that these acids occur in the gingival crevices of human subjects with severe periodontal disease at millimolar levels which are > 10-fold higher than those found in mildly diseased subjects, and are undetectable in healthy subjects. Further, when applied directly to healthy human gingiva, short-chain carboxylic acids stimulate a gingival inflammatory response and inflammatory cytokine release, At the cellular level, these acids inhibit proliferation of gingival epithelial and endothelial cells, and inhibit leukocyte apoptosis and function, but can stimulate leukocyte cytokine release. At the molecular level, these acids can stimulate neutrophil gene transcription, translation, and protein expression. Thus, the likelihood is high that these acids, in addition to their cariogenic activity, can promote and prolong gingival inflammation.Our challenge will be to identify the cell or cells of the periodontium which respond to short-chain carboxylic acids, to delineate their responses and the molecular mechanism(s) of these effects, and to categorize the aspects of the inflammatory components which damage and those which protect the host. With this information, it may be possible to begin to rationally identify and test pharmaceutical agents which diminish the harmful aspects, while enhancing the beneficial components, of the inflammatory response.

show abstract

“…The degree of saturation with respect to hydroxyapatite (DS) was calculated to be 0.94. This corresponds with DS values in pooled plaque fluid derived from exposed root surfaces of caries-active subjects [Gao et al, 2001;Margolis et al, 1993]. Separate demineralization solutions were used for all groups and replaced after 3 and 6 days.…”

mentioning

confidence: 99%

Influence of Olive Oil Emulsions on Dentin Demineralization in vitro

et al. 2003

View full text Add to dashboard Cite

The effect of two different concentrations of olive oil emulsions on development of artificial caries-like dentin lesions under severe demineralizing conditions was investigated. Bovine dentin samples (n = 180) were ground flat, polished, divided into four groups, and subjected to three demineralization cycles per day. Samples were stored in one of the following solutions for 5 min prior to demineralization in a buffer solution (pH 5): Group 1: 50% oil emulsion (olive oil and distilled water); group 2: 5% oil emulsion; group 3: distilled water; and group 4: 1,500 ppm sodium fluoride. Daily up to 9 days, lesion depth (ld) and mineral loss (ΔZ) were determined by means of microradiography and analyzed by ANOVA and Tukey’s studentized range test (p ≤ 0.05). Lesion depth increased with time for all groups. Mineral loss increased in groups 1–3. A small but significant decrease in mineral loss was observed following treatment with lipid emulsions as compared to treatment with distilled water, but fluoride treatment was considerably more effective. Mean mineral loss (means ± SD in vol%·µm) averaged over the study period was 4,368 ± 1,599, 4,536 ± 1,823, 4,849 ± 1,798, and 789 ± 177 for group 1, 2, 3, and 4, respectively. Ratio (ΔZ/ld) remained constant around 30 vol% for groups 1–3, but decreased for group 4. In conclusion, externally provided lipids have the potential to reduce dentin demineralization in vitro.

show abstract

Cariogenic potential of pooled plaque fluid from exposed root surfaces in humans

Cited by 17 publications

References 25 publications

Clearance and Metabolism of Starch Foods in the Oral Cavity

Clearance and Metabolism of Starch Foods in the Oral Cavity

Short-Chain Carboxylic-Acid-Stimulated, PMN-Mediated Gingival Inflammation

Influence of Olive Oil Emulsions on Dentin Demineralization in vitro

Contact Info

Product

Resources

About